Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000524060 | SCV000621912 | pathogenic | not provided | 2017-10-19 | criteria provided, single submitter | clinical testing | The c.3109_3110delTC variant in the KMT2D gene has not been reported previously as a pathogenic variant nor as a benign variant, to our knowledge. The variant causes a frameshift starting with codon Serine 1037, changes this amino acid to a Proline residue, and creates a premature Stop codon at position 30 of the new reading frame, denoted p.Ser1037ProfsX30. This variant is predicted to cause loss of normal protein function either through protein truncation or nonsense-mediated mRNA decay. The c.3109_3110delTC variant is not observed in large population cohorts (Lek et al., 2016). We interpret c.3109_3110delTC as a pathogenic variant. |
Labcorp Genetics |
RCV002528291 | SCV003335270 | pathogenic | Kabuki syndrome | 2022-03-27 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 453057). This variant has not been reported in the literature in individuals affected with KMT2D-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Ser1037Profs*30) in the KMT2D gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in KMT2D are known to be pathogenic (PMID: 22126750). |